Bootsma D, Westerveld A, Hoeijmakers J H
Department of Cell Biology and Genetics, Erasmus University, Rotterdam.
Cancer Surv. 1988;7(2):303-15.
The genetic disease xeroderma pigmentosum (XP) demonstrates the association between defective repair of DNA lesions and cancer. Complementation analysis performed on XP cell strains and on repair deficient rodent cell lines has revealed that at least nine and possibly more than 13 genes are involved in early steps of the excision of ultraviolet light-induced DNA lesions in mammalian cells. Two of these genes have been cloned and others are in an advanced stage of cloning. One cloned gene, ERCC-1, has been characterized at the molecular level. This human gene is homologous with excision repair genes in yeast and in Escherichia coli. These results indicate that the excision repair system is conserved during evolution. It is expected that the cloning and characterization of prokaryotic and eukaryotic repair genes will pave the way to a deeper understanding of mammalian repair systems and their association with cancer.
遗传性疾病着色性干皮病（XP）显示了DNA损伤修复缺陷与癌症之间的关联。对XP细胞株和修复缺陷的啮齿动物细胞系进行的互补分析表明，至少9个且可能超过13个基因参与了哺乳动物细胞中紫外线诱导的DNA损伤切除的早期步骤。其中两个基因已被克隆，其他基因正处于克隆的后期阶段。一个已克隆的基因ERCC-1已在分子水平上得到表征。这个人类基因与酵母和大肠杆菌中的切除修复基因同源。这些结果表明，切除修复系统在进化过程中是保守的。预计原核生物和真核生物修复基因的克隆和表征将为更深入了解哺乳动物修复系统及其与癌症的关联铺平道路。
